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A 2-AP probe is used to replace ssDNA-FQ in the classical CRISPR/Cas12 system, realizing the highly sensitive detection of nucleic acids by the CRISPR/Cas12 system with the screened 2-AP probe as a reporter.

Yuan, Fangzhengyuan, Zhexue Qin, Chuan Liu, Shiyong Yu, Jie Yang, Jun Jin, Shizhu Bian, Xubin Gao, Jihang Zhang, Chen Zhang, Mingdong Hu, Jingbin Ke, Yuanqi Yang, Jingdu Tian, Chunyan He, Wenzhu Gu, Chun Li, Rongsheng Rao, and Lan Huang. Echocardiographic right ventricular outflow track notch formation and the incidence of acute mountain sickness.

BACKGROUND In the patients with AECOPD, the gut displays ischemia, anoxia and oxidative stress, which lead to the intestinal barrier failure. Therefore, it is desirable to screen for effective intestinal barrier-related biomarkers to monitor the disease severity. METHODS We conducted a prospective observational study in 40 patients with AECOPD and 10 patients with stable COPD. The serum levels of I-FABP, citrulline, D-Lactate, DAO, and α-GST, as well as the APACHE II scores were recorded. Person correlation analysis, logistic regression models and receiver operating characteristic (ROC) curve analyses were used in our study. RESULTS Patients with AECOPD had significantly higher levels of I-FABP, D-Lactate, and DAO than did those with stable COPD. However, the serum citrulline level was significantly decreased in the patients with stable COPD than in those with AECOPD and the serum α-GST was not significantly changed. Additionally, we observed that there was a higher levels of I-FABP, D-Lactate, and DAO and a lower level of citrulline in patients with severe COPD than in patients with nonsevere COPD [APACHE II (nonsevere COPD)

High altitude (HA) exposure has been considered as a cardiac stress and might impair ventricular diastolic function. Atrial contraction is involved in ventricular passive filling, however the atrial performance to HA exposure is poorly understood. This study aimed to evaluate the effect of short-term HA exposure on bi-atrial function. Physiological and 2D-echocardiographic data were collected in 82 healthy men at sea level (SL, 400 m) and 4100 m after an ascent within 7 days. Atrial function was measured using volumetric and speckle-tracking analyses during reservoir, conduit and contractile phases of cardiac cycle. Following HA exposure, significant decreases of reservoir and conduit function indexes were observed in bi-atria, whereas decreases of contractile function indexes were observed in right atrium (RA), estimated via RA active emptying fraction (SL 41.7 ± 13.9% vs. HA 35.4 ± 12.2%, p = 0.001), strain during the contractile phase [SL 13.5 (11.4, 17.8) % vs. HA 12.3 (9.3, 15.9) %, p = 0.003], and peak strain rate during the contractile phase [SL − 1.76 (− 2.24, − 1.48) s−1 vs. HA − 1.57 (− 2.01, − 1.23) s−1, p = 0.002], but not in left atrium (LA). In conclusion, short-term HA exposure of healthy individuals impairs bi-atrial performance, mostly observed in RA. Especially, atrial contractile function decreases in RA rather than LA, which seems not to compensate for decreased ventricular filling after HA exposure. Our findings may provide a novel evidence for right-sided heart dysfunction to HA exposure. Supplementary Information The online version of this article (10.1007/s10554-021-02173-8) contains supplementary material, which is available to authorized users.

Objective. Coronavirus disease 2019 (COVID-19) is a considerable global public health threat. This study sought to investigate whether blood glucose (BG) levels or comorbid diabetes are associated with inflammatory status and disease severity in patients with COVID-19. Methods. In this retrospective cohort study, the clinical and biochemical characteristics of COVID-19 patients with or without diabetes were compared. The relationship among severity of COVID-19, inflammatory status, and diabetes or hyperglycemia was analyzed. The severity of COVID-19 in all patients was determined according to the diagnostic and treatment guidelines issued by the Chinese National Health Committee (7th edition). Results. Four hundred and sixty-one patients were enrolled in our study, and 71.58% of patients with diabetes and 13.03% of patients without diabetes had hyperglycemia. Compared with patients without diabetes ( n = 366 ), patients with diabetes ( n = 95 ) had a higher leucocyte count, neutrophil count, neutrophil to lymphocyte ratio (NLR), and erythrocyte sedimentation rate (ESR). There was no association between severity of COVID-19 and known diabetes adjusted for age, sex, body mass index (BMI), known hypertension, and coronary heart disease. The leucocyte count, NLR, and C-reactive protein (CRP) level increased with increasing BG level. Hyperglycemia was an independent predictor of critical (OR 4.00, 95% CI 1.72-9.30) or severe (OR 3.55, 95% CI 1.47-8.58) COVID-19, and of increased inflammatory levels (high leucocyte count (OR 4.26, 95% CI 1.65-10.97), NLR (OR 2.76, 95% CI 1.24-6.10), and CRP level (OR 2.49, 95% CI 1.19-5.23)), after adjustment for age, sex, BMI, severity of illness, and known diabetes. Conclusion. Hyperglycemia was positively correlated with higher inflammation levels and more severe illness, and it is a risk factor for the increased severity of COVID-19. The initial measurement of plasma glucose levels after hospitalization may help identify a subset of patients who are predisposed to a worse clinical course.

Objective: this study aimed to explore the impacts of myocardial injury on the clinical severity and outcomes in patients with Coronavirus Disease 2019 (COVID-19).Methods: we analyzed the electronic medical records of 1646 COVID-19 inpatients in Wuhan Huoshenshan Hospital. Results: 327 (19.9%) developed into severe cases, 23 (1.4%) died. In comparison to common cases, severe cases showed older age, more comorbidities, abnormal immune responses, as well as liver, renal, cardiac and coagulation disorders. Multivariable logistic regression identified that older age , combining with arrhythmia, abnormal lymphocyte percentage, elevated hypersensitive C reactive protein (hs-CRP) and myocardial injury were the independent risk factors for the incidence of severe cases. Moreover, Kaplan-Meier survival analysis showed that patients with myocardial injury had increasing risks of mortality, incidence of severe cases, acute respiratory distress syndrome (ARDS), and intensive care unit (ICU) admission. Particularly, myocardial injury patients co-existed with any other risk factor further deteriorated the clinical outcomes.Conclusion: The presence of myocardial injury and its co-existing with older age, arrhythmia, abnormal lymphocyte percentage, or elevated hs-CRP were greatly associated with the incidence of severe patients and poor clinical outcomes.

Background High altitude exposure induces overload of right-sided heart and may further predispose to supraventricular arrhythmia. It has been reported that atrial mechanical dyssynchrony is associated with atrial arrhythmia. Whether high altitude exposure causes higher right atrial (RA) dyssynchrony is still unknown. The aim of study was to investigate the effect of high altitude exposure on right atrial mechanical synchrony. Methods In this study, 98 healthy young men underwent clinical examination and echocardiography at sea level (400 m) and high altitude (4100 m) after an ascent within 7 days. RA dyssynchrony was defined as inhomogeneous timing to peak strain and strain rate using 2D speckle-tracking echocardiography. Results Following high altitude exposure, standard deviation of the time to peak strain (SD-TPS) [36.2 (24.5, 48.6) ms vs. 21.7 (12.9, 32.1) ms, p Conclusion Our data for the first time demonstrated that high altitude exposure causes RA dyssynchrony in healthy young men, which may be secondary to increased pulmonary arterial pressure. In addition, subjects with higher RA dyssynchrony presented worse RA contractile function and right ventricular performance.

Background: Coronavirus disease 2019 (COVID-19) patients with a larger ratio of pneumonia lesions are more likely to progress to acute respiratory distress syndrome and death. This study aimed to investigate the relationship of baseline parameters with pneumonia lesions on admission, as quantified by an artificial intelligence (AI) algorithm using computed tomography (CT) images. Methods: This retrospective study quantitatively assessed lung lesions on CT using an AI algorithm in 1630 consecutive patients confirmed with COVID-19 on admission and classified the patients into none (0%), mild (>0–25%), intermediate (>25–50%), and severe (>50%) groups, according to the lesion ratio of the whole lung. A multivariate linear regression model was established to explore the relationship between the lesion ratio and laboratory parameters. The baseline parameters associated with lung lesions, including demographics, initial symptoms, and comorbidities, were determined using a multivariate ordinal regression model. Results: The 1630 patients confirmed with COVID-19 had a median whole lung lesion ratio of 4.1%, and the right lower lung lobe had the most lesions among the five lung lobes based on the evaluation of CT using AI algorithm. The whole lung lesion ratio was associated with the levels of plasma fibrinogen (r=0.280, pConclusions: Based on AI-enabled CT quantitation, patients with initial symptoms of cough/shortness of breath, or with comorbidities of hypertension, diabetes, or anemia, had a higher risk for more severe lung lesions on admission in COVID-19 patients.

An excessive immune response contributes to SARS-CoV, MERS-CoV and SARS-CoV-2 pathogenesis and lethality, but the mechanism remains unclear. In this study, the N proteins of SARS-CoV, MERS-CoV and SARS-CoV-2 were found to bind to MASP-2, the key serine protease in the lectin pathway of complement activation, resulting in aberrant complement activation and aggravated inflammatory lung injury. Either blocking the N protein:MASP-2 interaction or suppressing complement activation can significantly alleviate N protein-induced complement hyper-activation and lung injury in vitro and in vivo. Complement hyper-activation was also observed in COVID-19 patients, and a promising suppressive effect was observed when the deteriorating patients were treated with anti-C5a monoclonal antibody. Complement suppression may represent a common therapeutic approach for pneumonia induced by these highly pathogenic coronaviruses.One Sentence SummaryThe lectin pathway of complement activation is a promising target for the treatment of highly pathogenic coronavirus induced pneumonia.

Background: Coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to spread worldwide, with high infectivity and mortality rates. The global pandemic poses a serious risk to public health and is of significant concern to the medical community. The current study was performed to delineate the clinical characteristics of cases with redetectable viral RNA post-discharge following hospital discharge during the quarantine period. Methods: Data on 51 patients with laboratory-confirmed COVID-19 were extracted through March 2, 2020. Findings: Median age was 57·0 (21–90) years, and 43% patients were female. Median time from initial symptoms to first discharge was 28 days and nine days from discharge to redetectable viral RNA. All patients were symptom-free, except one case presenting with fever and two with cough. Basic disease was observed in 47·1% patients, with hypertension being the most common manifestation. Laboratory and radiological findings were normal for the majority of patients. The median titers of anti-viral IgM and IgG antibodies in COVID-19 patients were 23·19 AU/mL and 170·36 AU/mL, respectively. No significant differences were observed between patients classified into the “persistence” and “non-persistence” groups based on the status of RNA positivity. The median length of hospital stay for patients that had reached the composite endpoint was 16·5 d and nine days in the persistence and non-persistence groups, respectively. Interpretation: The viral RNA for some symptom-free patients post-discharge can be positive with normal T cell subset and detectable IgG. More attentions should be paid to patients with re-detectable RNA of COVID-19. Funding Statement: None. Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: This study was approved by the Ethics Committee of the Army Medical University. Written informed consent was waived in light of the urgent need to collect clinical data

Autophagy plays a key role in pulmonary vascular remodeling via regulation of apoptosis and hyperproliferation of pulmonary arterial endothelial cells, which are the subject of increased attention. Autophagy-related 101 (ATG101) is an essential gene for the initiation of autophagy. Although the structure of ATG101 has been well-characterized, its exact biological function in autophagy is still unknown. In this study, an ATG101 single-stranded antisense RNA-loaded DNA triangular nanoparticle (ssATG101-TNP) is constructed to knock down the ATG101 gene expression. ssATG101-TNP can be effectively transfected into human pulmonary arterial endothelial cells (HPAECs) in time- and dose-dependent manners. Knockdown of ATG101 promotes cell apoptosis as well as inhibits cell autophagy and proliferation with hypoxic stimulation. Additionally, the hedgehog/Gli signal pathway is involved in ATG101-mediated macroautophagy and HPAEC proliferation. This study found that ATG101, an important member of the autophagy gene family, can regulate cell macroautophagy, apoptosis, and growth in HPAECs. ssATG101-TNP is demonstrated to be a nontoxic, highly efficient, gene-delivery vehicle for HPAECs. These findings also suggest that ATG101 might be a potential therapeutic target in diseases involving endothelial injury.

Peroxisome proliferator-activated receptor gamma (PPARγ) and miR-124 have been reported to play important roles in regulation of inflammation. However, the underlying anti-inflammatory mechanisms remain not well understood. In the present study, we demonstrated that the expression level of PPARγ is positively correlated with that of miR-124 in patients with sepsis. Activation of PPARγ upregulates miR-124 and in turn inhibits miR-124 target gene. PPARγ bound directly to PPRE in the miR-124 promoter region, and enhanced the promoter transcriptional activity. PPARγ-induced miR-124 is involved in the suppression of pro-inflammatory cytokine in vitro and in vivo. These results suggest that PPARγ-induced miR-124 inhibits the production of pro-inflammatory cytokines is a novel PPARγ anti-inflammatory mechanism and also indicate that miR-124 may be a potential therapeutic target for the treatment of inflammatory diseases.

High-altitude deacclimatization syndrome (HADAS) is involved in hypoxia-reoxygenation injury and inflammatory response, induced a series of symptoms, and has emerged as a severe public health issue. Here, we investigated the mechanism as well as potential means to prevent HADAS using Shenqi pollen capsules (SPCs) in subjects with HADAS in a multicenter, double-blinded, randomized, placebo-controlled study. All subjects were at the same high altitude (3650 m) for 4-8 months before returning to lower altitudes. Subjects (n=288) in 20 clusters were diagnosed with mild or moderate HADAS on the third day of the study. We randomly allocated 20 clusters of subjects (1 : 1) to receive SPCs or a placebo for 7 weeks, and they were then followed up to the 14th week. The primary endpoints were subjects’ HADAS scores recorded during the 14 weeks of follow-up. Compared with the placebo, SPC treatment significantly decreased the subjects’ HADAS scores and reduced the incidence of symptom persistence. SPC therapy also reduced the serum levels of CK, CK-MB, LDH, IL-17A, TNF-α, and miR-155 and elevated IL-10 and miR-21 levels. We thus demonstrate that SPCs effectively ameliorated HADAS symptoms in these subjects via suppression of the hypoxia-reoxygenation injury and inflammatory response.

Online Methods Supplement; Tables; Figures 1. Online Methods Supplement. 1.1 Section S1: Study Subjects: Inclusion and Exclusion Criteria. 1.2 Section S2: Randomization. 1.3 Section S3: Blinding and Quality Control. 1.4 Section S4: Study Methods. 2. Online Tables: 2.1 Table S1: Subgroup Analysis. 1.2 Table S2: Inclusion Number for Each Center per Year. 3. Online Figures: 3.1 Figure S1: The Daily Ventilation Time of NIV. 3.2 Figure S2: The maximum levels of IPAP (above EPAP) and EPAP Use during NIV. (PDF 376 kb)

Background: Travelling to high altitude (HA) presents a risk of the high levels of pulmonary artery pressure (PAP) at altitude, which is associated with impaired exercise capacity and fatal HA pulmonary oedema. However, prediction of high levels of PAP at altitude is still unclear. Methods: Echocardiography and pulmonary function tests were performed on 121 healthy men at low altitude (LA) and 4100 m (5 ± 2 h after a 7 day ascent). Results: HA exposure increased the levels of FEV1/FVC ratio, FEF25%, 50%, 75%, MMEF, mPAP, total pulmonary vascular resistance (PVR) and systolic pulmonary arterial pressure (SPAP). More smokers and lower forced expiratory flow at 25% of forced vital capacity (FEF25%) at LA were observed in subjects with mPAP≥30 mmHg than those with mPAP Conclusions: Thus, these findings suggest that subjects with low FEF25% values at LA are susceptible to high levels of PAP at altitude but not the incidence of AMS following short-term HA exposure, especially in smokers.

Silent mating type information regulation 2 homolog-1 (SIRT1) is involved in a wide range of cellular processes because of its role as a deacetylated histone and its association with a variety of transcription factors. SIRT1 has essential roles in autophagy, including in the formation of autophagic vacuoles and the assembly of autophagy-related gene (ATG) protein complexes. The present study focused on the role of SIRT1 in autophagy in lipopolysaccharide (LPS)-induced mouse type II alveolar epithelial cells (AECII). We designed experiments using SIRT1-overexpressing mice and wild-type mice, and AECII were isolated from these two types of mouse for in vitro LPS injury trials. Our results suggest that levels of the autophagy proteins, Beclin1 and LC3B, as well as those of the inflammatory factors, IL-6 and TNF-α, were increased in LPS-induced mouse AECII, and that SIRT1 protected against damage in mice with acute respiratory distress syndrome and in mouse AECII in vitro following LPS treatment. Subsequently, we screened multiple inflammatory, apoptotic, and unclassified genes (including Atg7), which interacted with SIRT1 in LPS-injured mouse AECII, as assessed by mRNA microarray analysis. These results demonstrate that LPS can reduce the levels of SIRT1 and ATG7 in vivo and in vitro and indicate that SIRT1 is involved in autophagy through regulation of ATG7 in AECII in response to LPS.

Rab5 GTPase modulates the trafficking of the cell surface receptors, including G protein-coupled β-adrenergic receptors (β-ARs). Here, we have determined the role of Rab5 in regulating the internalization of β-ARs in lung microvascular endothelial cells (LMECs) and in maintaining the integrity and permeability of endothelial cell barrier. Our data demonstrate that lipopolysaccharide (LPS) treatment disrupts LMEC barrier function and reduces the cell surface expression of β-ARs. Furthermore, the activation of β-ARs, particularly β2-AR, is able to protect the LMEC permeability from LPS injury. Moreover, siRNA-mediated knockdown of Rab5 inhibits both the basal and agonist-provoked internalization of β-ARs, therefore, enhancing the cell surface expression of the receptors and receptor-mediated ERK1/2 activation. Importantly, knockdown of Rab5 not only inhibits the LPS-induced effects on β-ARs but also protects the LMEC monolayer permeability. All together, these data provide strong evidence indicating a crucial role of Rab5-mediated internalization of β-ARs in functional regulation of LMECs.

The aim of this study was to separate, purify, and identify Salmonella paratyphi A flagellin, and to prepare its antisera. Primary flagellin was isolated from S. paratyphi A using the acid lysis method. The flagellin was purified with weak anion exchange chromatography and the protein was identified with sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), Western blot, and negative staining with phosphotungstic acid with scanning electron microscopy (SEM). The production of the obtained flagellin was then quantified. New Zealand white rabbits were then immunized with the isolated flagellin, the presence of serum anti-flagellin antibodies was assessed with the immunoblot test, and its potency was determined with the double immunodiffusion test. The results of SDS-PAGE showed that the molecular weight (m.w.) of the purified flagellin was 52 x 10(3). The immunoblot test also showed a band at 52 x 10(3) m.w. The SEM results showed that the flagellin was filamentous. These three results showed that the protein was homogeneous. The protein quantification analysis found that 4.8 ± 0.5 mg flagellin could be extracted per 1 g wet weight bacteria. The titer of the anti-flagellin antiserum was 1:64. Through this method, we obtained high productions of flagellin, which could be easily purified, identified, and prepared into high titer antiserum.

The aim of this study was to optimize the extraction parameters of Fomes officinalis Ames polysaccharides (FOAPs) and evaluate their antitumor activity. FOAPs were extracted using the hot water extraction, acid extraction and alkali extraction methods, respectively. Alcohol precipitation and acetone washes were conducted to separate and purify the FOAPs. The FOAP content was determined using the phenol-sulfuric acid method. The effects of raw material particle size, extraction time and material-liquid ratio on the yield of FOAPs were investigated, and the effects of FOAPs on the immune function of S180 tumor-bearing mice and their antitumor activity were evaluated. The yield of FOAPs obtained with the hot water extraction method was higher compared with the yields of the other methods. The optimum extraction conditions were as follows: a raw material particle size of 24 mesh; an extraction time of 2.5 h; and a material-liquid ratio of 1 g:12 ml. Under these conditions, the yield of FOAPs was 1.13%. FOAPs significantly inhibited tumor growth and enhanced the immune function in S180 tumor-bearing mice. FOAPs extracted using the hot water extraction method have antitumor activity.

High-altitude deacclimatization syndrome (HADAS) is emerging as a severe public health issue that threatens the quality of life of individuals who return to lower altitude from high altitude. In this study, we measured serum levels of SOD, MDA, IL-17A, IL-10, TNF-α, and HADAS score in HADAS subjects at baseline and 50th and 100th days and to evaluate the relationship between interleukins, including IL-17A, and HADAS. Our data showed that and the serum IL-17A levels and HADAS score decreased over time in the HADAS group, and serum IL-17A levels were significantly higher in the HADAS group at baseline and 50th day compared with controls (p<0.05). Furthermore, baseline serum levels of MDA and TNF-αwere significantly higher, while SOD and IL-10 levels were lower in HADAS subjects compared with controls (p<0.05). It is interesting that serum levels of IL-17A were clearly interrelated with HADAS incidence and severity (p<0.05). ROC curve analysis showed that combined serum IL-17A and IL-10 levels were a better predictor of HADAS incidence than serum levels of IL-17A or IL-10 alone. These data suggest that serum levels of IL-17A are a novel predictive index of HADAS.

Uncoupling protein 2 (UCP2) is upregulated in patients with systemic inflammation and infection, but its functional role is unclear. We up- or downregulated UCP2 expression using UCP2 recombinant adenovirus or the UCP2 inhibitor, genipin, in lungs of mice, and investigated the mechanisms of UCP2 in ALI. UCP2 overexpression in mouse lungs increased LPS-induced pathological changes, lung permeability, lung inflammation, and lowered survival rates. Furthermore, ATP levels and mitochondrial membrane potential were decreased, while reactive oxygen species production was increased. Additionally, mitogen-activated protein kinases (MAPKs) activity was elevated, which increased the sensitivity to LPS-induced apoptosis and inflammation. LPS-induced apoptosis and release of inflammatory factors were alleviated by pretreatment of the Jun N-terminal kinase (JNK) inhibitor SP600125 or the p38 MAPK inhibitor SB203580, but not by the extracellular signal-regulated kinase (ERK) inhibitor PD98059 in UCP2-overexpressing mice. On the other hand, LPS-induced alveolar epithelial cell death and inflammation were attenuated by genipin. In conclusion, UCP2 increased susceptibility to LPS-induced cell death and pulmonary inflammation, most likely via ATP depletion and activation of MAPK signaling following ALI in mice.

The presence of lung cancer cells in anoxic zones is a key cause od chemotherapeutic resistance. Thus, it is necessary to enhance the sensitivity of such lung cancer cells. However, loss of efficient gene therapeutic targeting and inefficient objective gene expression in the anoxic zone in lung cancer are dilemmas. In the present study, a eukaryotic expression plasmid pUC57-HRE-JAB1 driven by a hypoxia response elements promoter was constructed and introduced into lung cancer cell line A549. The cells were then exposed to a chemotherapeutic drug cis-diamminedichloroplatinum (C-DDP). qRT-PCR and western blotting were used to determine the mRNA and protein level and flow cytometry to examine the cell cycle and apoptosis of A549 transfected pUC57-HRE-JAB1. The results showed that JAB1 gene in the A549 was overexpressed after the transfection, cell proliferation being arrested in G1 phase and the apoptosis ratio significantly increased. Importantly, introduction of pUC57-HRE-JAB1 significantly increased the chemotherapeutic sensitivity of A549 in an anoxic environment. In conclusion, JAB1 overexpression might provide a novel strategy to overcome chemotherapeutic resistance in lung cancer.

Oral glucocorticoids can prevent acute mountain sickness (AMS). Whether inhaled budesonide (BUD) can prevent AMS remains unknown.Our aim was to investigate the effectiveness of BUD in AMS prevention.Eighty subjects were randomly assigned to receive budesonide (BUD, inhaled), procaterol tablet (PT), budesonide/formoterol (BUD/FM, inhaled), or placebo tablet (n = 20 in each group). Subjects were treated for 3 days before ascending from 500 m to 3700 m within 2.5 h by air. Lake Louis AMS questionnaire, blood pressure, heart rate, and oxygen saturation (SpO2) were examined at 20, 72, and 120 h after high-altitude exposure. Pulmonary function was measured at 20 h after exposure.Compared with placebo, BUD significantly reduced the incidence of AMS (70% vs. 25% at 20 h, p0.05; both 10% vs. 5% at 72 and 120 h, both p0.05) without side effects. The relative risk was 0.357, and the risk difference was 0.45. Mean SpO2 was higher in BUD, BUD/FM, and PT groups than in the placebo group at 20 h (p0.05). SpO2 in all 80 subjects dropped after ascent (98.1% to 88.12%, p0.01) and increased gradually, but it was still lower at 120 h than at baseline (92.04% vs. 98.1%, p0.01). Pulmonary function did not differ among the four groups at 20 h.BUD can prevent AMS without side effects. The alleviation of AMS may be related to increased blood oxygen levels rather than pulmonary function.

Several studies have investigated the association between Cyclin D1 (CCND1) G870A genetic polymorphism and lung cancer susceptibility, but the results were inconclusive. The aim of this meta-analysis was to summarize available evidence for such a relationship. The reviewers made use of MEDLINE, EMBASE, and BIOSIS databases. The relevant data were independently extracted by two reviewers. The odds ratio (OR) with 95% confidence interval (CI) was selected as the principal outcome measure. The heterogeneity test, the publication bias test, and the sensitivity analysis were performed. Overall, a total of 10 case-control studies were included. Our meta-analysis indicated that CCND1 G870A genetic polymorphism was a risk factor for lung cancer under homozygote model (OR = 1.18; 95% CI = 1.02, 1.37), recessive model (OR = 1.21; 95% CI = 1.03, 1.41), and allele model (OR = 1.11; 95% CI = 1.02, 1.21). In the subgroup analysis by source of ethnicity, a statistical increase of lung cancer risk was found among Asian groups for allele model (OR = 1.11; 95% CI = 1.01-1.22). The present meta-analysis suggests that CCND1 G870A polymorphism may be a risk factor for lung cancer. Besides, allele A may contribute to increased lung cancer risk.